Fig. 9.6 ), is particularly important with regard to the stretch reflex. These interneurons are identifiable because they are the only inhibitory interneurons •Fig. 9.6 Reflex Arc of the Stretch Reflex. Thepathwaybacktotherectusfemorisinthisarccontainsasinglesynapsewithinthecentralnervoussystem;hence,itisamonosynapticreflex.Theinterneuron,showninblack, isagroupIainhibitoryinterneuron.DRG,dorsalrootganglion.
that receive input from both the group Ia afferent fibers and Renshaw cells (see
Fig. 9.12 ). They end on α motor neurons that innervate the antagonist muscles—in this case, the hamstring muscles, including the semitendinosus muscle—which act to flex the knee. Other branches of the group Ia afferent fibers synapse with yet other neurons that originate ascending pathways that provide various parts of the brain (particularly the cerebellum and cerebral cortex) with information about the state of the muscle.
The organization of the stretch reflex arc guarantees that one set of α motor neurons is activated and the opposing set is inhibited. This arrangement is known as reciprocal innervation. Although many reflexes involve such reciprocal innervation, this type of innervation is not the only possible organization of a motor control system; descending motor pathways can override such patterns.
The stretch reflex is quite powerful, in large part because of its monosynaptic nature. The power of this reflex also derives from the essentially maximal convergence and divergence that exist in this pathway, which is not apparent from the circuit diagrams, such as
Fig. 9.6 , that are typically used to illustrate reflex pathways. That is, each group Ia fiber contacts virtually all homonymous α motor neurons, and each such α motor neuron receives input from every spindle in that muscle. Although its monosynaptic nature makes the group Ia reflex rapid and powerful, it also means that there is relatively little opportunity for direct control of
CHAPTER 9 Organization of Motor Function activity flow through its reflex arc. The CNS overcomes this problem by controlling muscle spindle sensitivity via the γ motor neuron system as described previously.
The Tonic Stretch Reflex
The tonic stretch reflex can be elicited by passive bending of a joint. This reflex circuit includes both group Ia and group II afferent fibers from muscle spindles. Group II fibers make monosynaptic excitatory connections with α motor neurons, but they also excite them through disynaptic and polysynaptic pathways. Normally, there is ongoing activity in the group Ia and group II afferent fibers that helps maintain a baseline rate of firing of α motor neurons; therefore, the tonic stretch reflex contributes to muscle tone. Its activity also contributes to the ability to maintain a posture. For example, if the knee of a soldier standing at attention begins to flex because of fatigue, the quadriceps muscle is stretched, a tonic stretch reflex is elicited, and the quadriceps contracts more, thereby opposing the flexion and restoring the posture.
The foregoing discussion suggests that stretch reflexes can act like a negative-feedback system to control muscle length. By following the stretch reflex arc, it is possible to see that changes in its activity act to oppose changes in muscle length from a particular equilibrium point. For example, if the muscle’s length is increased, there will be an increase in firing by group Ia and group II fibers, which excites homonymous α motor neurons and leads to contraction of the muscle and reversal of the stretch. Similarly, passive shortening of the muscle unloads the spindles and leads to a decrease in the excitatory drive to the motor neurons and thus relaxation of the muscle. So how are humans able to rotate their joints? It is partly because the γ motor neurons are coactivated during a movement and thereby shift the equilibrium point of the spindle and partly because the gain or strength of the reflex is low enough that other input to the motor neuron can override the stretch reflex.